The PI3K/Akt pathway is required for LPS activation of microglial cells
Abstract
Upregulation of inflammatory responses in the brain is associated with a number of neurodegenerative diseases. Microglia are activated in neurodegenerative diseases, producing pro-inflammatory mediators. Critically, lipopolysaccharide (LPS)-induced microglial activation causes dopaminergic neurodegeneration in vitro and in vivo. The signaling mechanisms triggered by LPS to stimulate the release of pro-inflammatory mediators in microglial cells are still incompletely understood. To further explore the mechanisms of LPS-mediated inflammatory response of microglial cells, we studied the role of phosphatidylinositol 3-kinase (PI3K)/Akt signal transduction pathways known to be activated by toll-like receptor-4 signaling through LPS. In the current study, we report that the activation profile of LPS-induced pAkt activation preceded those of LPS-induced NF-κB activation, suggesting a role for PI3K/Akt in the pathway activation of NF-κB-dependent inflammatory responses of activated microglia. These results, providing the first evidence that PI3K dependent signaling is involved in the inflammatory responses of microglial cells following LPS stimulation, may be useful in preventing inflammatory based neurodegenerative processes.
Autore Pugliese
Tutti gli autori
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CIANCIULLI A.;PANARO M.A.;CALVELLO R.
Titolo volume/Rivista
Non Disponibile
Anno di pubblicazione
2012
ISSN
0892-3973
ISBN
Non Disponibile
Numero di citazioni Wos
31
Ultimo Aggiornamento Citazioni
Non Disponibile
Numero di citazioni Scopus
31
Ultimo Aggiornamento Citazioni
Non Disponibile
Settori ERC
Non Disponibile
Codici ASJC
Non Disponibile
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